Chapter 16
the glucagon response to hypoglycemia: Blood glucose returns
toward normal, and fatty acids are supplied for cell utilization.
Cortisol, the major glucocorticoid produced by the adrenal
cortex, plays an essential permissive role in the adjustments
to fasting. We have described how fasting is associated with
the stimulation of both gluconeogenesis and lipolysis; how-
ever, neither of these critical metabolic transformations occurs
to the usual degree in a person defi cient in cortisol. In other
words, the plasma cortisol level does not need to increase
much during fasting, but the presence of cortisol in the blood
maintains the concentrations of the key liver and adipose tis-
sue enzymes required for gluconeogenesis and lipolysis (e.g.,
HSL). Therefore, in response to fasting, people with a cortisol
defi ciency develop hypoglycemia serious enough to interfere
with cellular function. Moreover, cortisol can play more than
a permissive role when its plasma concentration does increase,
as it does during stress. At high concentrations, cortisol elic-
its many metabolic events ordinarily associated with fasting
Table 16–3
). In fact, cortisol actually reduces the sensitivity
of muscle and adipose cells to insulin, which helps to main-
tain plasma glucose levels during fasting, thereby providing a
regular source of energy for the brain. Clearly, here is another
hormone, in addition to glucagon and epinephrine, that can
exert actions opposite those of insulin. Indeed, people with
very high plasma levels of cortisol, due either to abnormally
high secretion or to glucocorticoid administration for medical
reasons, can develop symptoms similar to those seen in indi-
viduals, such as certain diabetics, whose cells do not respond
properly to insulin.
Growth Hormone
The primary physiological effects of growth hormone are to
stimulate both growth and protein synthesis. Compared to
these effects, those it exerts on carbohydrate and lipid metab-
olism are minor. Nonetheless, as is true for cortisol, either
severe defi
ciency or marked excess of growth hormone does
produce signifi cant abnormalities in lipid and carbohydrate
metabolism. Growth hormone’s effects on these nutrients, in
contrast to those on protein metabolism, are similar to those
of cortisol and opposite those of insulin. Growth hormone
(1) renders adipocytes more responsive to lipolytic stimuli,
(2) increases gluconeogenesis by the liver, and (3) reduces the
ability of insulin to cause glucose uptake by muscle and adi-
pose tissue. These three effects are often termed growth hor-
mone’s “anti-insulin effects.” Because of these effects, some of
the symptoms seen in people with acromegaly (excess growth
hormone production; Chapter 11) are similar to those seen in
people with insulin resistance.
Sketetal muscle
Adipose tissue
Plasma epinephrine
Adrenal medulla
Epinephrine secretion
Plasma glucose
Plasma glucose, fatty acids, glycerol
Reflex via glucose receptors
in the central nervous system
Activity of sympathetic nerves
to liver and adipose tissue
Figure 16–10
Participation of the sympathetic nervous system in the response to a low plasma glucose concentration (hypoglycemia). Glycogenolysis in
skeletal muscle contributes to restoring plasma glucose by releasing lactate and pyruvate, which are converted to glucose in the liver. Recall
also from Figure 16–8 and the text that the sympathetic nervous system inhibits insulin and stimulates glucagon secretion, which further
contributes to the increased plasma fuel sources.
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